During the
development of the SFEMG method, a number of small but often rather useful help
tools or “gadgets” as some call them have been developed or at least tested for
use in clinical neurophysiology. They may have been more fun than useful, but
in some instances survived, even into commercially available equipment.

In order to see short duration signals, say
1 ms, that occur with a frequency of 10/sec, i.e. they occupy 1% of the time,
it is necessary to use a high display sweep speed, often 02-0.5 ms/div. In more
advanced oscilloscopes a trigger was built in, i.e. the sweep started when the
signal had reached an amplitude level that could be optionally adjusted. This
was not being used in clinical neurophysiology at the time and we could not
trigger on the SFAP. It should be noted that the trigger function is present
today in all EMG equipment. The default is that all signals with an amplitude
exceeding the trigger level start the sweep. We sophisticated the trigger
function further by introducing an amplitude window, so that the sweep started
as usual when the amplitude was high enough, but was inhibited if the amplitude
exceeded another higher amplitude. The amplitude window could be adjusted
optionally during the recording. This made it possible to separate signals that
had a lower amplitude than the highest (Czekajewski, Ekstedt, Stålberg 1969).
This feature has been included in some EMG equipment, but I think that the
possibilities it offers have not yet been sufficiently recognized. Another
problem was that only signal segments coming after the time of trigger could be
displayed on the sweep. This can be seen in some of our early figures. This was
solved by using a delay-line, see below.

The problem with the missing part before
the trigger had to be solved. We tried to use a tape recorder with separate
recording and reading heads. They are separated by 1-2 cm and by using the
correct tape speed; a delayed signal should be obtained. This was not a
practical solution - another type of delay line was necessary. Our first
solution was to use a one kilometer 14 paired cable. We connected the ends and
got a line of 28 km. This gave a delay of 93 µsec, sufficient to see some
significant early parts of the signal. This later became an electronic delay
with resistors and condensers, and later a digital delay, now the standard in
all EMG equipment (Czekajewski, 1969).

During
the development of SFEMG we needed to prove that we were able to record from
single muscle fibers. How to achieve this in human?

Fibrillation
potentials
are usually considered to be generated by individual fibers, so by recordings
from such signals we could determine their characteristics – good similarity to
our SFEMG signals.

Another
trick was to inject intramuscularly a small dose of sodium citrate. This
will chelate the sodium ions and fibers start to fire independent of each
other. A weak pain is felt.

Theoretically
partial curarization should be a method. At the initial stage of
neuromuscular block of the voluntary activated signal, individual building blocks
(signals from single muscle fibers) can be seen. When the jitter increased
individual components in possible compound signal started to show increased
jitter and often increased latency. Thus single fiiber action potential (a.p.)
revealed themselves as single fiber a.p. With further effect of the curare,
these jittering components also show intermittent and then complete block, The
all-or-none behavior strongly indicated that the spike was from a single muscle
fiber. It is a very short moment when this occurs and therefore this technique
never became a practical method to prove single fiber characteristics. Often
however, the spiky signal under exploration showed an all-or-none behavior upon
curarization, i.e. was present or absent. This was used as a strong indicator
of a recording from a single muscle fiber.

In
1978 we gave an EMG course in Bombay (Willison-England, Trojaborg -Denmark and
me-Sweden). One evening we were kindly invited to Mr Engineer’s for dinner. He
had also invited Ravi Shankar, relatively early in his career. All of us,
around 30 persons, were seated on the floor to listen to his music performed
on sitar and some other instruments played by Mr Shankar’s companions. Since
the listening group was large and the space quite big, a loudspeaker was placed
at the end of the room. Robin Willison was sitting close to this loudspeaker,
perhaps 15 m away from the players. A wonderful evening.

Next
morning, Dr Willison had a comment on the sound quality. He hear the muscle
both directly, with the normal delay for sound in air 50 msec for the 15 m, and
from the loudspeaker, which produced the sound without delay. His ear was very
annoyed by this dual, non-simultaneous sound input.

I
well remember when they described the trick of using different delays for the
sound to loudspeakers in Westminster Abbey; those speakers far away from the
pulpit had a longer delay than those placed closer to the pulpit.

The
opposite situation occurred in our laboratory. During a visit to us by Dr.
Jasper Daube, he pointed out that a problem he had with the EMG they used (at
that time a Neuromatic 2000, the same as ours), which gave an annoying time
difference between the signal display and the sound could not be detected in
our lab.

This
EMG machine had a technical feature to first record a signal segment for the
total display time, say 20msec. Not until after 20 msec was the trace displayed
on the screen, while the sound was “on line,” in real time. With a very slow
sweep, you could easily note this, but with short sweep times only an expert
like Daube could detect this. In our situation, often using a sweep time of 20
msec, we had free standing loudspeakers placed 3-6 m away (different for
different rooms) instead of the inbuilt speaker. Therefore the sound was
delayed (time through air) by about 10-20 msec, throughout the range of sweep
speeds that we used in routine. We should have had a system by which the
loudspeakers moved, depending on the sweep speed!

Together
with Dr. Hilton-Brown, I was visiting Columbus, Ohio in the late 70’ies. We
discussed EMG (what else?) while walking on the street. Intrigued by McComas’
relatively new publications on MUNE, we asked if that method could be improved.
His method was to use a metal strip as the surface electrode over the muscle,
usually small and thin muscles, such as ADM or EDB. Our own studies had shown
how motor units deep in a large muscle such as biceps, did not give a signal to
a surface electrode. Was there a way to get a large metal electrode inside the
muscle, close to the MU? Well, for EMG with concentric needle electrodes (our
standard) we always have a large piece of metal inside the muscle – the cannula
of the needle. So, on the street in Columbus we decided to use the cannula for
recording. Back home we made such recordings with a SFEMG electrode, triggering
on the SFEMG action potential and averaging the time-locked cannula signal. We
found that the amplitude depended on the depth of the electrode. (By the way,
this cannula signal is usually subtracted from the tip-recorded signal in EMG.
Since superficial positions of the electrode give larger cannula signals, more
will be subtracted in EMG, and a superficial MU will be seen with a lower
amplitude. We therefore modified the SFEMG electrode by Teflon insulation except
for the distal 15 mm, which gives a large but standardized recording surface as
long as the electrode is inserted at least 15 mm. The triggering SFEMG
electrode was placed 7.5 mm behind the tip, in the center of the bare part of
the cannula. This then became the classic Macro EMG setup.

Over the years I
have experienced in a couple of important and breath-taking moments.

One was the
decrement and jitter in rabbits that had developed antibodies to ACh-receptor.
This was the first clue of postsynaptic receptor involvement in MG (Heilbronn E,
Mattsson C, Stålberg E. Immune response in rabbits to a cholinergic receptor
protein: possibly a model for myasthenia gravis. Proc 3rd int cong on Muscle
Diseases, Newcastle 1974). The report came out just after the report
by Lennon
VA, Lindstrom JM, Seybold ME. Experimental autoimmune myasthenia: A model of
myasthenia gravis in rats and guinea pigs. J Exp Med 1975; 141:1365-1375

A memorable moment
in my scientific life was when in Oct 1991 we were asked to examine two
patients brought to Uppsala from the Congo. They had acute spastic paraparesis
and the pathophysiology was unknown. Insufficiently dried cassava had produced
cyanide poisoning with irreversible symptoms. They were brought to Uppsala.
For these patients, accompanied by family doctors and some locals, this event
must have been a shock. Flying in an airplane, coming to a hospital,
instruments giving electric shocks, and the noise in MRI. The hospital staff did
its best to understand their situation and help them adapt.

Blood chemistry -
normal. Imaging techniques - normal. A full EDX revealed no abnormalities in
motor or sensory nerves. EEG was normal in one and of low amplitude in the
other patient. But when it came to transcortical magnetic stimulation, we got
the clue. No responses from arm or legs. The conclusion was cortical
inexcitability in this disease, which was called Konzo. The studies continued
and led to Dr Tshalas’ doctoral thesis. Later Dr Karin Eeg-Olofson and eng PO
Fällmar from Uppsala went to Zaire for field studies. Local education on the
cause was implemented.

This
was the last day of an SFEMG course in Chapel Hill NC, US in 1987 held in an
anatomy auditorium. At the end of my good-bye speech I tripped backwards and
banged into the wall behind. This was assembled by swinging segments about 2 m
wide. Each segment could rotate around its vertical middle axis. I pushed one
segment which rotated 180 degree and I came into a small pitch dark room. At
the same time I heard laughter and applause. I had really not said anything
funny, but perhaps my exit was funny enough. When I after a short moment return
in front of the wall, I saw a skeleton, hanging on the back of the segment, now
widely exposed. The course really had a happy end.